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Lipid metabolism of liquid-associated and solid-adherent bacteria in rumen contents of dairy cows offered lipid-supplemented diets.

The lipid distribution and fatty acid (FA) composition of total lipids, polar lipids and free fatty acids (FFA) were determined in liquid-associated bacteria (LAB) and solid-adherent bacteria (SAB) isolated from the rumen contents of seven dairy cows fitted with rumen fistulas. Two experiments, arranged according to a 4 x 4 and 3 x 3 Latin Square design, were performed using two basal diets consisting of one part hay and one part barley-based concentrate, and five lipid-supplemented diets consisting of the basal diet plus (g/kg dry matter):53 or 94 rapeseed oil, 98 tallow, 87 soya-bean oil or 94 palmitostearin. For all diets used, total lipids were 1.7-2.2 times higher in SAB than in LAB (P less than 0.05); this probably resulted from a preferential incorporation of dietary FA absorbed onto food particles. Addition of oil or fat to the diets did not modify the polar lipid content but increased the FFA content of SAB and LAB by 150%. Lipid droplets were observed in the cytoplasm in SAB and LAB using transmission electron microscopy, which suggested that part of the additional FFA was really incorporated into the intracellular FFA rather than associated with the cell envelope by physical adsorption. Linoleic acid was specifically incorporated into the FFA of SAB, which emphasized the specific role of this bacterial compartment in the protection of this acid against rumen biohydrogenation.

Animals↗

Replacing dietary fish oil by vegetable oils has little effect on lipogenesis, lipid transport and tissue lipid uptake in rainbow trout (Oncorhynchus mykiss).

In order to investigate the effects of dietary lipid sources on mechanisms involved in lipid deposition, two groups of rainbow trout were fed from first-feeding to the commercial size of 1 kg (for 62 weeks) with two diets differing only by lipid source: 100% fish oil or 100% blend of vegetable oils (55% rapeseed oil, 30% palm oil, 15% linseed oil). The activities and levels of gene expression of lipogenic enzymes (fatty acid synthetase, glucose-6-phosphate dehydrogenase and malic enzyme) in liver and of lipoprotein lipase in perivisceral adipose tissue, white muscle and liver were determined. Transport of lipid was studied by determining lipid composition of plasma and lipoprotein classes. We also examined the clearance of LDL by assaying the level of LDL receptor gene expression in several tissues. Total replacement of dietary fish oil by the blend of vegetable oils did not affect growth of rainbow trout and did not modify muscle lipid content. Hepatic lipogenesis and lipid uptake in perivisceral adipose tissue, white muscle and liver were also not modified by dietary treatments. Diets containing the blend of vegetable oils induced a decrease in plasma cholesterol and LDL. In trout fed the vegetable oils diet, expression of LDL receptor gene in the liver was down-regulated.

Animal Nutritional Physiological Phenomena↗

Effects of alpha-tocopherol and beta-carotene on hepatic lipid peroxidation and blood lipids in rats with dietary iron overload.

The ability of dietary antioxidants to reduce lipid peroxidation induced by iron overload was examined in weanling male Sprague-Dawley rats. Animals were fed ad libitum a modified AIN-76A diet (control) or control diet with 0.5% alpha-tocopherol acid succinate, 0.5% crystalline trans-beta-carotene, or 0.5% alpha-tocopherol acid succinate + 0.5% trans-beta-carotene for four weeks. In the following four-week period, the animals received the above diets with 10,000 micrograms Fe/g; a control group continued to receive 35 micrograms Fe/g, and a high-iron group received 10,000 micrograms Fe/g with no antioxidants. After four weeks of dietary supplementation with alpha-tocopherol. Beta-carotene or alpha-tocopherol + beta-carotene, liver concentrations of alpha-tocopherol and beta-carotene increased significantly (p < 0.001). Liver lipid peroxidation, measured by the lipid-conjugated diene assay, increased significantly from 0.012 mumol/mg of lipid in the controls to 0.021 mumol/mg of lipid in animals receiving the high-iron diet. However, lipid peroxidation was significantly reduced in all animals fed the antioxidants, with the group fed alpha-tocopherol + beta-carotene having a lower level than the high-iron group. Total serum cholesterol was elevated in animals fed a high-iron diet and in animals fed the high-iron diet with alpha-tocopherol. In contrast, total serum cholesterol levels in the two groups of animals receiving the diets containing high iron with beta-carotene alone or high iron with beta-carotene + alpha-tocopherol were significantly reduced to the level of the control group. High-density lipoprotein cholesterol also decreased to baseline in the animals receiving beta-carotene alone. Modulation of lipid peroxidation by alpha-tocopherol or beta-carotene may be an important mechanism for reducing oxidative stress.

Animals↗

Effects of vitamin E deficiency and nitrogen dioxide exposure on lung lipid peroxidation: use of lipid epoxides and malonaldehyde as measures of peroxidation.

The effect of vitamin E deficiency in male Sprague-Dawley rats upon lipid peroxidation in lung tissue was examined by measuring malonaldehyde and lipid epoxide production. In addition to controls, some animals were also exposed to 3 +/- 0.1 ppm NO2 continuously for 7 d in order to study the effects of oxidant stress on lung lipid peroxidation and vitamin E content. The observed changes in malonaldehyde and epoxide content could serve as good indices of lipid peroxidation, particularly under conditions of vitamin E deprivation. The responses measured indicated an inverse relation in the lung between tissue vitamin E content and quantity of lipid peroxidation products. Measurement of lipid epoxides served as a reliable indicator of lung tissue lipid peroxidation. Finally, NO2 inhalation appeared to elicit a response characterized by increased assimilation of vitamin E into lung tissue.

Animals↗

Co-association of cytochrome f catabolites and plastid-lipid-associated protein with chloroplast lipid particles.

Distinguishable populations of lipid particles isolated from chloroplasts of yellow wax bean (Phaseolus vulgaris L. cv Kinghorn Wax) leaves have been found to contain plastid-lipid-associated protein (J. Pozueta-Romero, F. Rafia, G. Houlné, C. Cheniclet, J.P. Carde, M.-L. Schantz, R. Schantz [1997] Plant Physiol 115: 1185-1194). One population is comprised of plastoglobuli obtained from sonicated chloroplasts by flotation centrifugation. Higher density lipid-protein particles isolated from chloroplast stroma by ultrafiltration constitute a second population. Inasmuch as the stromal lipid-protein particles contain plastid-lipid-associated protein, but are distinguishable from plastoglobuli in terms of their lipid and protein composition, they appear to be plastoglobuli-like particles. Of particular interest is the finding that plastoglobuli and the higher density lipid-protein particles both contain catabolites of the thylakoid protein, cytochrome f. These observations support the view that there are distinguishable populations of plastoglobuli-like particles in chloroplasts. They further suggest that the formation of these particles may allow removal of protein catabolites from the thylakoid membrane that are destined for degradation as part of normal thylakoid turnover.

Amino Acid Sequence↗

Intravascular lung macrophages play an essential role in lipid entrapment and the inflammatory tissue reaction seen after long-term lipid-based parenteral nutrition in pigs. An ultrastructural study.

To detect possible interactions between lipid-based total parenteral nutrition (TPN) substrates and mononuclear phagocytes, ultrastructural in vitro and in vivo studies were carried out on material from pigs. Mononuclear phagocytes isolated from peripheral blood, phagocytosed lipid after incubation with 1 mg/ml Intralipid for 24 h. Similarly, lipid was taken up by intravascular macrophages in the lungs and liver after central venous administration of TPN containing 2.3 g/kg body weight/day of Intralipid for 5-7 weeks. Lipid accumulation was almost exclusively found intravascularly in the lungs and liver, and not in macrophages obtained from bronchoalveolar lavage fluid. A morphometric study of the lung capillaries showed that the macrophages in TPN animals had increased in size and number, and occupied a larger portion of the capillary lumina. The macrophages appeared to be activated, but the endothelial lining was well preserved. Free intravascular lipid droplets had a diameter both in vitro and in vivo of about 0.5 micron, indicating good stability of the emulsion. We suggest that the lipid uptake stimulates the macrophages and thereby plays a role in the lung tissue inflammation seen in response to long-term lipid-based TPN in pigs.

Animals↗

Lipids in total parenteral nutrition solutions differentially modify lipids in piglet intestinal brush border and microsomal membranes.

BACKGROUND: Fats in the diet modify the lipid composition and function of the intestinal brush border membrane (BBM) as well as the enterocyte microsomal membrane (EMM). METHODS: This study was undertaken in pigs to establish the effect of 3 weeks of total parenteral nutrition (TPN) on the fatty acids in the major phospholipids, (phosphatidylcholine [PC] and phosphatidylethenolamine [PE] in the jejunal and ileal BBM and EMM. RESULTS: In a comparison of 21-day-old milk-fed piglets and newborn animals, there were differences in the major fatty acids (palmitic, 16:0; stearic, 18:0; oleic, 18:1 omega 9, and linoleic acid, 18:2 omega 6) in PC and PE in BBM and EMM. Age-matched (3-week-old) animals fed a lipid-free glucose-containing TPN solution had different membrane fatty acids than did milk-fed piglets, or animals given a soybean oil-containing TPN solution for 21 days. Substituting fish oil or fish oil plus soybean oil altered BBM and EMM fatty acids, compared with the soybean oil-based TPN solutions. These changes varied between the class of phospholipids (PC vs PE), between intestinal site (jejunum vs ileum), and between the type of membrane (BBM vs EMM). CONCLUSIONS: The jejunum and ileum have distinctive control mechanisms for varying their membrane lipids in response to TPN. There is some postmicrosomal modification of lipids between the EMM and BBM. It remains to be established whether the lipid content of the membranes of other organs, and therefore their function, is modified by the lipid composition of parenterally infused lipids.

Aging↗

Labeled acetate incorporation into lipids and lipid elimination after oral administration in rat liver and adipose tissue.

To investigate the incorporation of acetate into fatty acids and their turnover, the time courses for the incorporation of labeled acetate into lipids in the liver and epididymal adipose tissue (adipose tissue) after the oral administration to rats were examined for 10 d. The labeled acetate was abundantly incorporated into lipids, mainly into triacylglycerols (TAG) in the liver, reached a maximum at 2 h after the administration and then quickly decreased. In the adipose tissue, the incorporation of the acetate reached a maximum after 8 h and began to decrease slowly after 2 d. The acetate incorporation into the lipids was markedly lower in the liver, plasma and adipose tissue of rats fed the corn oil diet than in those fed the fat-free diet. However, the half-lives of esterified fatty acids were similar in both dietary groups. The half-lives of esterified C16:0 and C18:1 in the decreasing phase were 5.4 and 8.9 h, respectively, in the liver, and 4.3 and 5.6 d, in the adipose tissue. The time courses for incorporation into plasma lipids were parallel to those in the liver. Thus the fatty acids synthesized in the liver appeared to be transported to adipose tissues and to stay there longer. Moreover, it is remarkable that 30% of the acetate radioactivities administered were found after 2 h in the whole liver: 75% of the products from the acetate at the maximum were lipids and 61%, of the lipids, TAG. The major products from acetate in the liver were lipids.

Acetates↗

Effects of oral contraceptive norethindrone on blood-lipid and lipid peroxidation parameters.

Considering importance of the lipophilicity of norethindrone (log P=2.97), a significant contributor to its mechanism of action, interaction of the drug with total lipids of goat whole blood have been investigated using phospholipid binding, fatty acid composition and peroxidation phenomena as the parameters under investigation. The objective was to derive an insight into the pharmacodynamic behavior of the drug by correlating biological activity with drug induced changes in lipid constituents. Significant loss in phospholipid along with changes in fatty acid cotmposition was observed after incubation of whole blood with norethindrone at 56 ng/ml (effective contraceptive concentration in blood) in varying periods of time. This may be ascribed to binding affinity of norethindrone with lipid constituents in blood. Lipid binding potential of the drug may have a role in its therapeutic effect. Lipid peroxidation induction potential of norethindrone was quantitatively measured in the context of its toxicity. The results reveal that northindrone caused significant extent of lipid peroxidation. Ascorbic acid, a promising antioxidant, at equivalent human dose levels of 250 mg and 500 mg could significantly reduce norethindrone induced lipid peroxidation.

Animals↗

[Plasma lipid profile and lipid peroxidation in overweight or obese children and adolescents].

OBJECTIVE: To study the plasma lipid profile and lipid peroxidation in overweight or obese children and adolescents receiving care at the pediatric endocrinology clinic in HOSPED/UFRN, a university hospital. METHODS: Three groups were studied: overweight (n = 15), obese (n = 30) and control (n = 21) children and adolescents. To evaluate plasma lipid profile, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglyceride levels were measured. Lipid peroxidation was determined by measuring malondialdehyde concentration. Data were analyzed using Student's t test, Tukey test, ANOVA and Pearson's correlation. RESULTS: Altered levels of total and LDL-cholesterol were observed mainly in overweight or obese males. HDL-cholesterol was borderline in the overweight and obese groups of both sexes. Obese females had the highest levels of triglycerides. Increased plasma lipid peroxidation was observed mainly in obese males. CONCLUSION: In the present population, the greatest alterations in lipid profile were observed in obese and overweight males. Plasma lipid peroxidation was more evident in obese males and females.

Adolescent↗

Pathogenesis of experimental lipid keratopathy: corneal and plasma lipids.

Corneal and plasma lipids were studied in a rabbit model to gain insight into the pathogenesis of secondary lipid keratopathy. Rabbits were divided into four groups in which a high cholesterol diet and corneal suture placement were varied to produce lipid keratopathy. In rabbits with lipid keratopathy, quantitative thin layer chromatography revealed that cholesterol esters comprised most of the deposited lipid, with free cholesterol being deposited as well. The ratio of accumulated cholesterol ester to free cholesterol corresponded closely to the same ratio in hypercholesterolemic plasma total low and very low density lipoprotein (TLDL). Furthermore, gas chromatography showed that the cholesterol ester composition in the corneas with lipid keratopathy resembled that seen in hypercholesterolemic plasma TLDL but was different from the pattern observed in the normal cornea. These studies suggest that the direct source of the deposited cholesterol ester is primarily the plasma TLDL. Since phospholipids and triglycerides did not show a significant increase in the experimental corneas, they are presumably metabolized by the keratocytes after the uptake of TLDL. However, the amount of cholesterol ester carried by the lipoprotein exceeds the capacity of the cell for use and excretion and the lipid accumulates in the cornea.

Animals↗

[Comparative study of lipid transfer between cell organelles using lipid-transfer proteins in vitro].

The transfer of de novo synthesized lipids from microsomes to lipid non-synthesizing membranes was studied in vivo and in vitro from the ratios of specific radioactivities of [14C]cholesterol, [14C] and [32P]phosphatidylcholine and [32P]phosphatidylethanolamine in the nuclei and mitochondria to that in microsomes. The radioactivity of lipids transferred from microsomes to mitochondria and nuclei was identical both in vitro and in vivo and when the lipid-exchange protein of the 105 000 g supernatant was used. Acceleration of lipid metabolism in the liver of gamma-irradiated rats was concomitant with the increase in the rate of labeled cholesterol transfer cation to liver cell nuclei and mitochondria, but remained unchanged in in vitro studies involving lipid-exchange protein. The reduction of phosphatidylethanolamine transfer to the nuclei in vitro and in vivo diminished in the same way. The existence in the cell of mechanisms of transfer of de novo synthesized cholesterol other than lipid-exchange protein is postulated.

Animals↗

Lipid peroxidation in autoimmune systemic vasculitides. Effect of corticoid treatment on lipid peroxidation. Antioxidant protection with vitamin E.

The effect of treatment with prednisone on lipid peroxidation and on lipid metabolism generally and the effect of vitamin E on plasma lipid peroxidation were studied in a group of patients with autoimmune systemic vasculitides. Vitamin E total plasma antioxidant capacity was determined to ascertain the antioxidant efficiency of vitamin E. Treatment with prednisone was found to induce disturbances of the lipid metabolism at the level of total cholesterol and of triglycerides. The increased values of the LDL/HDL ratio showed an increased risk of vascular disturbance in the patients investigated. The high level of lipid peroxides associated with a reduced activity of the endogenous antioxidant system was found to be uninfluenced by treatment with prednisone. Treatment with vitamin E reduced the process of lipid peroxidation but the endogenous deficiency of the antioxidant capacity prevented it to resume its normal values. In spite of the antiinflammatory and antioxidant treatment the high level of lipid peroxides might induce a self-maintained chronic process which, in time, might lead to the aggravation of the degenerative vascular changes.

Adult↗

Microchromatographic analysis of lipids, protein, and occurrence of lipid peroxidation in various brain areas of vanadium exposed rats: a possible mechanism of vanadium neurotoxicity.

Administration of sodium metavanadate (3 mg/kg) to adult female Sprague Dawley rats for 5 consecutive days by intraperitoneal route resulted in major alterations in lipid profiles and protein concentration in all the brain regions. Sodium metavanadate exposure displayed significant decrease in the levels of total lipids, phospholipids, cholesterol and cerebrosides, and protein, but ganglioside concentration was significantly increased in various areas of the brain. Loss of body weight observed in this study could be attributed to the loss of appetite; loss of nutrients and wasting of tissues. It is likely that large amount of body water was lost through diarrhoea. Gas liquid chromatography has revealed that oleic acid, linoleic acid, linolenic acid, and arachidonic acid were preferentially lost in the brain of vanadium-exposed rats. Thin layer chromatography further proved degradation of individual lipids. Sphingomyelin was substantially decreased followed by phosphatidyl choline and phosphatidyl ethanolamine, but phosphatidyl serine and phosphatidyl inositol were slightly affected. Our recent work has demonstrated vanadium-induced stimulation of lipid peroxidation in the various regions of the rat brain. It is speculative that deterioration of myelin sheath by vanadium exposure contributed to preferential lipid loss but lesser loss of protein. These studies also indicate that vanadium-induced stimulation of lipid peroxidation is characterized by a selective loss of brain polyunsaturated fatty acids and thus comprehensive degradation of lipids in the different regions of the rat brain. However, the mechanism involved in the elevation of ganglioside levels is not yet fully understood. It is concluded that these perturbations produced damage to the associated physiological functions leading to CNS functions.

Animals↗

[Lipids metabolism evaluated of by vitamin E to total lipid ratio in maternal and cord sera in normal pregnancy].

Changes in plasma levels of lipids peroxide (LPO) and vitamin E(VE) are observed in pregnant women. We measured levels of VE and lipids in 80 maternal and cord sera in normal delivery and obtained the following results. 1. For each lipid and VE, the concentration gradients were preserved in maternal sera to cord sera through placentas. 2. The concentration of VE correlated with that of total lipids (TL) in both sera. 3. The VE to TL ratio (VE/TL ratio) inversely correlated with the concentration of LPO in both sera. 4. The concentration of VE correlated with the VE/TL ratio and there was a more significant correlation of the VE and VE/TL ratio than that of VE and TL in both sera. 5. The VE/TL ratio in maternal serum correlated with VE/TL ratio and the concentration of VE in cord serum. These results suggested that lipids in serum was a regulatory factor in VE and that VE and lipids maintained the gradation of the concentration according to their own placental transport systems. It seems that the fetus has a unique VE which is comparatively lowered. This may be due to the effects of the accelerated lipid metabolism in the fetus.

Female↗

Effect of lipid peroxide loading on lipid peroxidation and on the glutathione and cytochrome systems in rabbits.

New Zealand White rabbits (6 males and 6 females) were fed a diet of high lipid peroxide content (peroxide value: 249.05 meq/kg fat) for 21 days. Twelve rabbits served as controls (peroxide value: 40.3 meq/kg fat). The lipid peroxide loading did not cause clinical signs. The rate of lipid peroxidation, as measured on the basis of thiobarbituric acid reactive substances (TBARS), was significantly (P < 0.05) higher in all of the investigated tissues, in the following order: liver > red blood cells (RBC) > blood plasma. Reduced and oxidised glutathione content was higher in the blood plasma (P < 0.01) and liver (P < 0.001) of rabbits exposed to the peroxide load. Lipid peroxide loading decreased the activity of glutathione peroxidase in the blood plasma, RBC haemolysate and liver and that of glutathione reductase in the liver. The amount of cytochrome P450 (both CO- and metyrapone-reduced) and the activity of cytochrome c (P450) oxidoreductase in the microsomal fraction of the liver homogenate were also lower in the group exposed to lipid peroxide load. Subchronic alimentary lipid peroxide loading in the presence of sufficiently high levels of antioxidants in the complete feed was found to increase the rate of lipid peroxidation and markedly lower the activities of both the glutathione and xenobiotic transforming enzyme systems without causing any clinical signs of toxicity.

Animals↗

Lipid-saccharide intermediates in glycoprotein biosynthesis. I. Formation of an oligosaccharide-lipid by thyroid slices and evaluation of its role in protein glycosylation.

Thyroid slices were found to incorporate radioactivity from 14C-labeled sugars into the carbohydrate moiety of a polar lipid soluble in chloroform/methanol/water, 10/10/3. This radiolabeled glycolipid was purified by chromatography on DEAE-cellulose and was shown to have as its monosaccharide constituents mannose, glucose, and glucosamine. This compound cloud also be labeled by incubation of thyroid slices with [3H]mevalonic acid or [32P]phosphate as demonstrated by the coincidence of elution profiles upon DEAE-cellulose chromatography. This suggested that the lipid portion of the molecule is a polyprenol derivative and the lipid-saccharide linkage region involves a phosphate bridge. Mild acid hydrolysis of the glycolipid labeled with 14C in its carbohydrate released a neutral oligosaccharide which on the basis of Bio-Gel filtration studies was shown to have a molecular weight of approximately 2,400. This oligosaccharide contained [14C]mannose and [14C]glucose in about the same ratio as that occurring in the intact glycolipid. The oligosaccharide-lipid appeared to be distributed rather widely in thyroid particulate fractions obtained after differential and density gradient centrifugation. Its highest specific activity occurred in fractions rich in endoplasmic reticulum. By means of pulse-chase experiments in slices a relationship was demonstrated between the disappearance of radioactivity from the lipid-bound oligosaccharide and its appearance in protein-bound form. When protein synthesis was inhibited by the addition of puromycin during the chase period of the experiment transfer of oligosaccharide from the lipid to protein appeared to be blocked and the level of radiolabeled oligosaccharide-lipid increased. The observation that mannose and glucose were similarly affected during the pulse-chase studies suggests that transfer of the intact oligosaccharide unit was involved in the addition of carbohydrate to protein.

Animals↗

Lipid-rich cell thyroid adenoma: histopathology with comparative lipid analysis.

A second case of the unique lipid-rich cell thyroid adenoma is described complemented by detailed lipid analysis. New observations were made. The cytoplasm of the tumour cells contained scattered, aggregated sudanophil crystals; under polarized light the frozen, unstained sections exhibited numerous birefringent lipid crystals; electron microscopy provided further evidence that the clear cell appearance was due to intracellular lipid droplets with scanty glycogen particles. Comparative lipid analysis by thin layer chromatography and high-pressure liquid chromatography (HPLC) revealed quantitative and qualitative differences in lipid composition of tumour cells when compared with goitre cells from normal thyroid gland and subcutane fat. Qualitative differences in triglyceride composition (by HPLC) between tumour cells and subcutaneous fat indicated that the fat accumulation in the follicle cells was not a result of simple storage, but an expression of altered intracellular lipid metabolism.

Adenoma↗